Abstract
A 54 years old male with undiagnosed chronic calcific degenerative aortic valve incompetence presented with acute left anterior chordae tendinae rupture resulting in severe left heart failure and cardiogenic shock. He was successfully treated with emergency double valve replacement using mechanical valves. The pathogenesis of acute rupture of the anterior chordae tendinae, without any evidence of infective endocarditis or ischemic heart disease seems to have been attrition of the subvalvular mitral apparatus by the chronic regurgitant jet of aortic incompetence with chronic volume overload. We review the literature with specific focus on the occurrence of this unusual event.
Highlights
Acute spontaneous rupture of the anterior chordae tendinae of a normal mitral valve leading to acute mitral incompetence is uncommon
This report is the first documentation of tricuspid calcific degeneration of the aortic valve with chronic incompetence leading to acute chordal rupture of the anterior mitral leaflet (AML)
Acute mitral incompetence is due to failure of the valve mechanism at annulus, leaflet or subvalvar level
Summary
Acute spontaneous rupture of the anterior chordae tendinae of a normal mitral valve leading to acute mitral incompetence is uncommon. This report is the first documentation of tricuspid calcific degeneration of the aortic valve with chronic incompetence leading to acute chordal rupture of the anterior mitral leaflet (AML). There was no past history of chronic renal failure, primary or secondary hyperthyroidism His initial clinical examination revealed him to be in atrial fibrillation with a fast ventricular rate. His Electrocardiogram showed voltage evidence of left ventricular hypertrophy with volume overload, but no evidence of acute, or old myocardial infarction. His basic blood investigations, creatinine kinase (CK-MB) and troponin I levels were normal. A transesophageal echocardiogram showed severe mitral incompetence due to chordal rupture with a flail anterior mitral leaflet (Figure 1) prolapsing into the left atrium (Figure 2). Histopathological examination of the excised valves and chordae showed central myxoid degeneration with chronic superficial fibrosis, [Figure 3] without the underlying cause being apparent
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